Abstract
Effects of carbon monoxide-releasing molecules on cGMP levels and soluble guanylate cyclase activity
Highlights
Carbon monoxide (CO) is a signaling molecule that controls many physiological processes in mammalian tissues
The CO-releasing molecules (CORMs)-stimulated increase was minor (50– 300% over basal) compared to the effects seen with the NO-donor, sodium nitroprusside (SNP)
CO and CORMs modestly reduced SNPstimulated cGMP formation in Rat aortic smooth muscle cells (RASMC)
Summary
Carbon monoxide (CO) is a signaling molecule that controls many physiological processes in mammalian tissues. CO gas activates sGC by 3–4-fold and exerts vasodilatory effects through elevation of cGMP. Certain transition metal carbonyls liberate CO in a controlled fashion and function as CO-releasing molecules (CORMs). Some of these agents have a variety of pharmacological effects and have yielded encouraging results in preclinical models, where CORM administration alleviates inflammatory processes and cardiovascular disorders. The aim of the present work was to investigate whether the pharmacological effects of CORMs could be attributed to sGC activation. To this end, we selected 12 CORMs and tested their ability to alter cGMP levels
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